IB Psychology students, welcome to the very, very strange world of the placebo.​

Our last IB Psychology blog post on nocebos generated a tonne of responses, and also a lot of questions. Some of our IB Psychology students concerned themselves with the fact that while we focused on the nocebo effect, we paid scant attention to the placebo effect ... it was almost as if we were assuming that every student of IB Psychology already had a good in-depth understanding of placebos and the placebo effect. And, to be honest, to some extent we were. The placebo effect is integral to the abnormal option and should feature heavily across multiple IB Psychology learning outcomes, including:

To what extent do biological, cognitive and sociocultural factors influence abnormal behaviour?

Evaluate the use of biomedical, individual and group approaches to the treatment of one disorder.

It really should be common knowledge. The placebo also takes a starring role in the IB Psychology CLOA learning outcome: To what extent do cognitive and biological factors interact in emotion? Where it features centrally in Schachter and Singer's (1962) two-factor theory of emotion. This piece of research can also be used in any of the IB Psychology exam questions that ask you to evaluate research or ethics at either the cognitive or biological level of analysis. So, as the astute amongst you have already worked out, you get quite good bang for your buck in the IB Psychology examinations by learning about placebos (work smarter, not harder!). So what are they?

Simply put, a placebo, as defined in IB Psychology, is a substance that has no therapeutic effect, and is used as a control in testing new drugs. However, that simple definition misses so much about the inner workings of the human mind. Placebo ares really, really strange beasts and they throw a whole lot of tricky questions at our knowledge and understanding of the human brain. See the must see video below.

WELCOME to the STRANGE world of the placebo

Without a doubt, placebos are one of the most interesting and perplexing concepts IB Psychology throws up. The concept also makes for a great IB Psychology Extended Essay, especially when confined a specific concept - such as the efficacy of selective serotonin reuptake inhibitors (SSRIs) in the treatment of depression. However, our focus here is on using the placebo effect in your IB Psychology abnormal option to help you achieve that elusive IB Psychology 7! To that end, here are some key concepts that can be memorised and included in your ERQs:

Kirsch et al. (2002) found that there was a publication bias in research into the effectiveness of SSRI in depression. In fact, if the results of all studies (including the ones that had not been published) were pooled together it would seem that the placebo effect accounted for 80% of the antidepressant response. A placebo is a substance that has no therapeutic effect, and is used as a control in testing new drugs. Of the studies funded by pharmaceutical companies, 57% failed to show a statistically significant difference between antidepressant and a neutral placebo. This and similar studies cast doubt on the serotonin hypothesis, not to mention the ethics of drug companies. However, it is still widely promoted by pharmaceutical companies and presumably believed by the 10% of Americans taking these SSRIs to treat depression.

Leauhter et al. (2002) examined changes in brain function during treatment with placebo. The study examined brain function in 51 patients with depression who either received placebo or an active antidepressant medication. An EEG was used to compare brain function in the two experimental groups. The design was double-blind and ran over none weeks. The study used two different SSRI, which were randomly allocated to participants.​Results showed a significant increase in activity in the prefrontal cortex nearly from in the beginning in the trial in the placebo group. The pattern was different from the patients who were treated with the SSRI but patients in both groups got better. This indicates that medication is effective, but placebo is just as effective. The findings from the study are intriguing. The difference in activity in the brain indicates that the brain is perhaps able to heal itself since there was a positive effect for both groups. Believing that they are being treated could be enough for many patients.

These concise and informative key paragraphs above, if reproduced in your IB Psychology exams, will have the examiner ticking all of the knowledge and critical thinking boxes available to her - ensuring you maximum marks!

​Remember, we take all of the guess work and all of the hard work out of IB Psychology with our especially prepared model IB Psychology exam answers.

Placebo or real? ... and more importantly, does it even matter?!

​The 60 Minutes segment embedded above provides the IB Psychology student with much insight into the role of placebos in medical research and just how much of the effects of antidepressant medications is probably attributable to the placebo effect (not to mention the pharmaceutical industry exploiting this in highly unethical ways).

We may have always intuitively understood the mind-stomach connection. Anxious? - butterflies in the stomach. Terrified? - Bring my brown pants. Disgust? - sick to he bottom of my stomach, and so on and such forth. Now some rather startling science is shedding some light onto this connection.

We have previously looked at the dreaded swim test, every lab rat's worst nightmare. Here it is used again to shed some light on a few different questions posed in the IB Psychology syllabus, both in the biological Level of Analysis and the Abnormal Psychology option.

The IB Psychology Biological Level of Analysis (BLOA) learning outcome: Discuss how and why particular research methods are used at the biological level of analysis (for example, experiments, observations, correlational studies). With the focus being a good experimental study. We can can also use it to address the IB Psychology Biological Level of Analysis (BLOA) learning outcome: Discuss two effects of the environment on physiological processes.

The hypothesis, good bacteria, in the right balance in the gut, will have positive effects on mental health - reducing stress and anxiety. To test this experimentally. Take two experimental groups of lab rats and manipulate an independent variable. One group is fed probiotics in their diet and the other a broth (a broth is cooked and thus has no bacteria, good or bad, present).

Choose the dependent variable, how long rats will keep swimming in a standard water maze (safe haven platform removed!) before giving up and going into a 'dead float'. Now this isn't actually the rats dying, they're just giving up on finding a way out of their stressful environment. No rats were harmed in the making of this experiment.

The results? Rats with a digestive system loaded with good bacteria did not give up. They continued to explore their environment looking for a way out until the experimenters took pity on them, lifted them out and gave them a fluffy towel and a quick blow dry. Those rats with less healthy gut flora gave up, en masse, within about two minutes. This is a classic sign of depression, less exploration and stress avoidance escape behaviour.

The conclusion, the good gut bacteria were somehow altering brain function in a positive way. Further experiments, this time with the unfortunate effects of euthanising the participants, pin pointed the vagus nerve - the vagus nerve is one of 12 cranial nerves, extending from the brain stem to the abdomen. When this was surgically severed, the probiotics conferred no such protective effects in stress avoidance or blood cortisol levels.

Use this study, embedded below, to address the IB Psychology Abnormal Psychology option learning outcome: Analyse etiologies of one disorder (major depression). As well as IB Psychology Abnormal Psychology option learning outcome: Evaluate the use of biomedical, individual and group approaches to the treatment of one disorder (again, major depression).

Feeling sad? Anxious about that party you are attending on the weekend? Simple answer ... get stuck into a big tub of healthy (and delicious) of natural yogurt. Yum yum!

A really funny, insightful and illuminating 15 minutes of Radiolab. Listening to this is guaranteed to send you straight out to your local supermarket to stock up on yogurt.

Of course, if you don't have time to prepare your own model IB Psychology exam questions, you can borrow ours! All answers to the IB Psychology extended response questions have been prepared for you. Full marks guaranteed!

In the IB Psychology Abnormal option we examine the effect of various biomedical approaches to the treatment of various psychological disorders. We examine the biomedical approach to the treatment of major depression under the following two learning outcomes:

Examine biomedical, individual and group approaches to treatment.

Evaluate the use of biomedical, individual and group approaches to the treatment of one disorder.

There are different biomedical treatments for depression that could be considered here, for example lobotomies and electroshock (electroconvulsive) therapy, but by far the most widely used biomedical approach to the treatment of major depression is the use of antidepressants. You are probably familiar with the brand names Prozac and Zoloft even if you have never had a sad day in your life. The biological mechanisms behind our most common (and effective) antidepressants seem grounded in sound science.

Serotonin is our brain's 'feel good' neurotransmitter, and by boosting serotonin levels in the brain we should be able to make our depressive patients feel a whole lot better about themselves and life in general. SSRIs, or selective serotonin re-uptake inhibitors, do exactly this, they inhibit the neurotransmitter serotonin from being reabsorbed back into the synapses where it was initially released, thus allowing for a build up of serotonin in the synaptic gap and an increase in activity in serotonergic neurons. What you will find once you dig deep enough is that this is incredibly controversial.

This question of biomedical treatments is examined in-depth in two model answers to the IB Psychology ERQs

And, when we start prescribing these medications to our children in ever increasing numbers you can be sure that serious questions are going to be raised. Consider the list of side effects of one of our most commonly prescribed SSRIs:

ARe America's Children Over-medicated?

The documentary above provides an informative and entertaining look into the world of psychotropic medications being prescribed to children in America.

Is the effectiveness of SSRIs due to the placebo effect? Reviewing the evidence we can conclude that using the most common antidepressant medications, the SSRIs such as Prozac and Zoloft are no more effective than taking a placebo. Moreover, reviewing the list of side effects, taking a placebo may be a whole lot safer!

The biomedical treatment of depressionThe biomedical approach to treatment is based on the assumption that if a mental problem is caused by biological malfunctioning, the cure is to restore the biological system with drugs. For example, the serotonin hypothesis of depression suggests that depression is linked to low levels of the neurotransmitter serotonin (Coppen, 1967). Serotonin is a neurotransmitter produced by specific neurons in the brain that are called serotonergic neurons because they produce serotonin. Antidepressant treatment should therefore aim to regulate serotonin levels. Antidepressants are often used in the treatment of bulimia nervosa because many patients also suffer from other disorders such as depression (the problem of comorbidity). Antidepressants are also used to treat minor depressive symptoms but the American Food and Drug Administration (FDA, 2004) warned that the use of antidepressants for children and adolescents could perhaps lead to an increased risk of suicide. In fact, the FDA adopted a "black box" label warning indicating that antidepressants may increase the risk of suicidal thinking and behaviour in some children and adolescents with major depression at about twice the rate of placebo. A black-box warning is the most serious type of warning in prescription drug labelling.Selective serotonin reuptake inhibitors (SSRIs)

Figure 1: SSRIs increase serotonin levels in the synaptic gap

Antidepressants in the form of selective serotonin reuptake inhibitors (SSRI) block the reuptake process for serotonin This results in an increased amount of the serotonin in the synaptic gap (see figure 1). The theory is that this increases serotonergic nerve activity leading to an improvement in mood. Essentially, the only evidence that exists in favour of the serotonin hypothesis is the alleged efficacy of SSRIs – if they make your serotonin more potent and this improves your condition, the problem must have been in your serotonin levels to begin with, or so the logic goes. According to Lacoste & Leo (2005) this is an example of backward reasoning. Assumptions about the causes of depression are based on how people respond to a treatment and this is logically problematic. For example, the symptoms of headaches can be treated by aspirin, but this is definitely not to say that the cause of headaches is a deficiency of aspirin.

SSRI drugs such as Prozac, Zoloft and Paxil are now amongst the most commonly prescribed antidepressants and this has been taken as indirect support for the serotonin hypothesis. They do affect mood and emotional responses positively in most people (although much of this may be due to the placebo effect; Kirsch et al., 2008). SSRIS have been criticised because they treat the symptoms of depression but do not cure the mental disorder, and because depressive episodes usually recur, it is necessary for patients to continue taking the medication. Unless the medication is used with therapy, it is unlikely that the disorder will disappear permanently.

However, SSRIs are popular because they have fewer side effects than previous drugs such as tricyclic antidepressants. Not everyone can use SSRIs and the most common side effects are headache, nausea, sleeplessness, agitation and sexual problems.

Neale et al. (2011) conducted a meta-analysis of published studies on the outcome of antidepressants versus placebo. The study focussed on: (i) patients who started with antidepressants and then changed to placebo, (ii) patients who only received placebo, and (iii) patients who only took antidepressants. The study found that patients who do not take antidepressants have a 25% risk of relapse, compared to 42% or higher for those who have been on medication and then stopped it.

According to the researchers, antidepressants may interfere with the brain’s self-regulation. They argue that drugs affecting serotonin or other neurotransmitters may increase the risk of relapse. The drugs reduce symptoms in the short-term but, when people stop taking the drug, depression may return because the brain’s natural self-regulation is disturbed.

Ingeniously, Henninger et al. (1996) performed experiments where they reduced serotonin levels in healthy individuals to see if they would develop depressive symptoms. The results did not support that levels of serotonin could influence depression; i.e., there was no evidence for a cause-effect relationship, and they argued that it was necessary to revise the serotonin hypothesis. This is strong evidence against the hypothesis because if low levels of serotonin do cause depression and they were successful in reducing serotonin levels in their participants (and the evidence presented suggests that this was the case), then this can be considered strong evidence against the serotonin-depression hypothesis. However, there has been debate around just how depression was monitored in this study.

Leauhter et al. (2002) examined changes in brain function during treatment with placebo. The study examined brain function in 51 patients with depression who either received placebo or an active antidepressant medication. An EEG was used to compare brain function in the two experimental groups. The design was double-blind and ran over none weeks. The study used two different SSRI, which were randomly allocated to participants.

Results showed a significant increase in activity in the prefrontal cortex nearly from in the beginning in the trial in the placebo group. The pattern was different from the patients who were treated with the SSRI but patients in both groups got better. This indicates that medication is effective, but placebo is just as effective. The findings from the study are intriguing. The difference in activity in the brain indicates that the brain is perhaps able to heal itself since there was a positive effect for both groups. Believing that they are being treated could be enough for many patients.

Kirsch et al. (2002) found that there was a publication bias in research into the effectiveness of SSRI in depression. In fact, if the results of all studies (including the ones that had not been published) were pooled together it would seem that the placebo effect accounted for 80% of the antidepressant response. A placebo is a substance that has no therapeutic effect, and is used as a control in testing new drugs. Of the studies funded by pharmaceutical companies, 57% failed to show a statistically significant difference between antidepressant and a neutral placebo. This and similar studies cast doubt on the serotonin hypothesis, not to mention the ethics of drug companies. However, it is still widely promoted by pharmaceutical companies and presumably believed by the 10% of Americans taking these SSRIs to treat depression.

In sum, when evaluating the evidence for the biomedical approach to the treatment of major depression we can conclude that SSRIs may reduce depressive symptoms but they have side effects and do not cure patients. It is likely that the placebo effect could account for the effectiveness of the medication. Further, because the mechanisms are not well understood not how antidepressants affect the brain in the long-term, it is possible that the heavy use of these could well be damaging. There is also increasing criticism of the role of pharmaceutical companies and their marketing of antidepressants, which has led to an increase in the prescription of SSRI.So parents, your kid is acting a little bit moody, disinterested and disengaged from her surrounds, should you be pushing your GP for some Prozac?

Have a read of the side effects of antidepressants in children and adolescents in the journal article below.

Black Magic - The Placebo Effect

Antidepressants are placebos

Black box warnings

side effects of SSRIs on children

If your answer to the above question was a resounding "No way!", based on the evidence that that they aren't effective, then you may have added reason to pat yourself on the back ... the FDA has also issued a 'black box' warning on all SSRI antidepressants. They found and believed it was in the public interest that those taking SSRIs be warned that there is an increased risk of suicidal thoughts or behavior (suicidality) in children and adolescents treated with SSRI antidepressant medications.

The black box warning, a type of warning issued by the FDA that must appear on the packaging of certain prescription drugs. The U.S. Food and Drug Administration (FDA) has required all pharmaceutical companies to place a boxed warning on the labeling of prescription antidepressants, or in literature describing it. It is the strongest warning that the FDA requires, and signifies that medical studies indicate that the drug carries a significant risk of serious or even life-threatening adverse effects.

In this instance, the FDA believes that already depressed children are more likely to commit suicide because taking these medications leads to the idea of suicide becoming more salient.

Consequently, prescriptions issued for antidepresants have fallen by over 20 per cent in the US.Now, this may seem a good thing in light of all of the evidence presented here. But consider this: during this time, child and adolescent suicides in the US jumped by 11 per cent! So, I'll leave you with this final thought ... should we now be prescribing a nice, safe placebo instead for a mental illness that has very real consequences for the sufferer?

Picture this. You are a mad scientist. You place a large number of rats into individual containers filled with water, get out the stop watch and time how long it takes them to succumb to the inevitable – death by drowning. And, as if this isn’t mad enough already, half of these rats you then rescue from their watery grave. You take them out, towel them off, give them a bit of a blow dry, reassure them that it was all just a terrible mistake, and give them some food, a blanket to warm themselves and a teddy bear to cuddle as they try to overcome their ordeal. Then, (ha ha!) you place them back into their watery containers and time how long it takes them to drown this time. For real. Didn’t I tell you that you were a mad scientist? [For the impatient among you, skip to the end for the fascinating AND repellant results.] A bizarre study has just landed on my desk. In the IB Psychology Diploma course we examine in detail the ethics of research studies in the learning outcome: Discuss ethical considerations related to research studies at the cognitive level of analysis (also at the biological and socio-cultural levels of analysis). And those choosing the Abnormal Psychology option (and that’s most of you out there) will probably look at major depression as an affective disorder, and explore the learning outcome: Analyse etiologies of one disorder. This study by Richter (1957) can be applied to both learning outcomes in IB Psychology. Firstly, there are (now) clear guidelines in the American Psychological Association (APA) manual into the ethical treatment of animals when used in research studies. Guidelines which were obviously lacking in 1957. The following ethical guidelines have now been formulated:

Animal research should try to avoid harm to animals. Any harm caused to animal should be carefully weighed against the research’s potential to provide significant benefit to the health or welfare of humans or other animals, or if it is unavoidable (e.g., electrodes that monitor individual neuronal hippocampal activity in memory tasks). If the procedure would cause pain to humans, it should be assumed that it will cause pain to animals. Animal welfare should be monitored and animals should be euthanised as soon as possible if research causes long term/serious harm and/or affects their ability to live normally and pain-free.

Now while the results of Richter the mad rat torturer are astonishing (yes, we’ll come to these in a minute), there is no way they could have been predicted ahead of time. No hypothesis was formed, it was just a see what happens ‘study’ which, incidentally, came to provide great insight into some factors that can lead to depression. Thus, it fails the “…research’s potential to provide significant benefit …” test. In fact, what Richter was really interested in was the sudden deaths associated with Voodoo cultures when a victim had been cursed – a tenuous connection to drowning rats at best. It also begs the question as to what else he was doing to animals that was not making it into the scientific literature (rescuing them from the mouths of feral cats before feeding them to rabid dogs?).

Further: “If the procedure would cause pain to humans, it should be assumed that it will cause pain to animals (APA).” Super stressed animals suffering a protracted death cannot possibly be justified here. Poor rats. Trust your gut instincts. If this was not your initial reaction then consider taking this test.

Unethical? Definitely. So what insight does the research provide us into the etiologies of major depression? Now, we need to look at those results.

Foolish rats! Haven't you heard of Dr Curt Richter?

The average length of time at which rats stopped swimming and drowned in the ‘helplessness’ condition was short. Rats in this condition ceased swimming and drowned within minutes – they just gave up, submitting to what they believed was inevitable.

The rescued rats swam for hours. Up to sixty hours of swimming, paddling and treading water was recorded in this dastardly study. Rescue a rat, provide them with some hope and they will fight and try and hang on in there until they have exhausted their physical and mental limits.

Warning! Contains graphic content

A cause of depression linked suicide is the phenomenon of learned helplessness. Learned helplessness is all about feeling trapped in an insoluble situation. A depressed person can believe that his or her situation is impossible to escape. Through experience, people can think, feel and behave as if their situation is helpless, when it is not. Repeated exposure to these negative thoughts, feelings and behaviours can lead to depressive thoughts, and eventually … well, we know how some people eventually believe they can find some control in their lives. Control over how they can ultimately escape the situation.

If you cannot find your own way out. You will need to reach out and find that helping hand. Let’s just hope that that hand doesn’t belong to a mad scientist.